ライフサイエンスコーパス: neurovascular

1 iously unrecognized effector of the damaging neurovascular actions of Abeta and unveil a new mechanis

2 is unclear whether tau contributes to these neurovascular alterations independent of neurodegenerati

3 egeneration, and provide a mechanism for the neurovascular alterations observed in the preclinical st

4 ings unveil a pathogenic role of PVMs in the neurovascular and cognitive dysfunction associated with

5 derstanding the complex interactions between neurovascular and neuroinflammatory responses in aging a

6 ovascular, urological, gastrointestinal, and neurovascular applications.

7 nd mature cells play in CNS angiogenesis and neurovascular barrier maturation have been elucidated in

8 on electrophysiological measurements free of neurovascular biases suggest that functional brain integ

9 Recent advances in neurovascular biology, epidemiology, brain imaging, and

10 Gli1+ PDLSCs are surrounding the neurovascular bundle and more enriched in the apical reg

11 ssessed the extent of soft tissue component, neurovascular bundle involvement, epiphyseal and joint i

12 luding areas of the prostate adjacent to the neurovascular bundles, the rectum, and the bladder wall.

13 We identify these channels as neurovascular canals, that include parts of the trigemin

14 phosphorylation, revealed similarities among neurovascular cell types, especially between BV-2 microg

15 duced by UGS and its components in different neurovascular cell types.

16 s in the therapeutic mechanisms in different neurovascular cell types.

17 found that UGS and its components protected neurovascular cells against diverse damaging agents and

18 unit and the therapeutic relationships among neurovascular cells should be defined.

19 ther with the functional connections between neurovascular cells, can explain the therapeutic effects

20 that include: (i) multi-contrast imaging of neurovascular changes following auditory stimulation; (i

21 In this study, we aimed to investigate early neurovascular changes using wild-type (WT) controls and

22 depends on the precise molecular control of neurovascular co-patterning.

23 ights into region-specific specialization of neurovascular communication, with special implications f

24 oosted in vivo by manipulating Flna-mediated neurovascular communication.

25 nding of the molecular mechanisms that cause neurovascular complications, particularly in type 2 diab

26 whole human dental pulp with emphasis on the neurovascular components.

27 rement, pain, loss of function and mobility, neurovascular compromise, and occasionally life-threaten

28 Neurovascular constriction was enhanced approximately 1.

29 f the diagnostic workup to detect a possible neurovascular contact and exclude secondary causes.

30 ension, an increased fibroblast growth rate, neurovascular contact at the rostral-ventrolateral medul

31 he prevalence and significance of trigeminal neurovascular contact in a large cohort of consecutive S

32 ical and therapeutic relevance of trigeminal neurovascular contact in short lasting unilateral neural

33 The proportion of neurovascular contact on the symptomatic trigeminal nerv

34 The odds on having neurovascular contact over the symptomatic nerves was si

35 Demonstration of a neurovascular contact should not be used to confirm a di

36 Our findings suggest that neurovascular contact with morphological changes is invo

37 On symptomatic nerves, neurovascular contact with morphological changes was cau

38 Neurovascular contact with morphological changes was def

39 tomatic side, indicated that the presence of neurovascular contact with morphological changes was str

40 Neurovascular contact with morphological changes were co

41 ding to the presence, location and degree of neurovascular contact.

42 change in internal carotid artery blood flow Neurovascular coupling (i.e. the relationship between lo

43 The classical model of neurovascular coupling (NVC) implies that activity-depen

44 inical models, yet the mechanisms underlying neurovascular coupling (NVC) in humans have yet to be el

45 G (aEEG) outputs impact the determination of neurovascular coupling (NVC) in newborns with encephalop

46 Neurovascular coupling (NVC) is the process whereby neur

47 Physiologically, neurovascular coupling (NVC) matches focal increases in

48 nimal models and the translation to critical neurovascular coupling (NVC) patterns for human fMRI.

49 a proof of concept study aiming to quantify neurovascular coupling (NVC) using wavelet analysis of t

50 They play an important role in mediating neurovascular coupling (NVC) via several astrocytic Ca(2

51 sodilatory prostaglandins play a key role in neurovascular coupling (NVC), the tight link between neu

52 utrients to active neurons, a process termed neurovascular coupling (NVC).

53 altered calcium signaling that could disrupt neurovascular coupling and gliotransmission.

54 may regulate experience-dependent changes in neurovascular coupling and myelination.

55 ions of mural cells in vascular development, neurovascular coupling and neuropathology.

56 ron, a direction opposite to that of classic neurovascular coupling and referred to here as vasculo-n

57 ting local blood vessels, a mechanism termed neurovascular coupling and the basis of BOLD functional

58 esponses to investigate cocaine's effects on neurovascular coupling and to differentiate its effects

59 001), indicating that cocaine did not affect neurovascular coupling at rest and that the reduction in

60 Neurovascular coupling between resting-state neural acti

61 Neurovascular coupling describes the link between neuron

62 min after cocaine injection, indicating that neurovascular coupling during stimulation was temporaril

63 he present study assessed CBF regulation and neurovascular coupling during submaximal cycling exercis

64 as reliable quantitative reporters to follow neurovascular coupling dynamics.

65 Second, neurovascular coupling ensures that, following local neu

66 future investigations on the impairments of neurovascular coupling from vascular diseases such as di

67 Early impairments to neurovascular coupling have been proposed to be a key pa

68 transcriptional regulator of SEMA3E-mediated neurovascular coupling in a mouse model of oxygen-induce

69 indicating that nitric oxide is integral to neurovascular coupling in humans.

70 n to assess the influence of nitric oxide on neurovascular coupling in humans.

71 Wavelet coherence analysis of neurovascular coupling in NE may identify infants at ris

72 transcriptional regulator of SEMA3E-mediated neurovascular coupling in pathological retinal angiogene

73 direct proportionality of volumetric spatial neurovascular coupling in the cerebral cortex.

74 Here, we investigate spatial correlations of neurovascular coupling in three dimensions, by applying

75 Mechanistically, the failure of neurovascular coupling involves a tau-induced dissociati

76 or functional brain imaging(2), and impaired neurovascular coupling is implicated in neurodegeneratio

77 location within the microvascular tree where neurovascular coupling is initiated, and the role of mur

78 Neurovascular coupling is the basis for functional brain

79 is needed for improving our understanding of neurovascular coupling mechanisms and the related measur

80 Together, our findings revealed a neurovascular coupling network that regulates experience

81 erlying molecular and cellular mechanisms of neurovascular coupling remain poorly understood.

82 Thus, neurovascular coupling remained preserved under a chroni

83 overed capillaries control vasomotion during neurovascular coupling remains controversial.

84 regulation of cerebral blood flow (CBF) and neurovascular coupling remains, however, under debate.

85 nitric oxide synthase inhibitor reduced the neurovascular coupling response by ~30%, indicating that

86 ling lead to a switch in the polarity of the neurovascular coupling response from vasodilation to vas

87 ies such as Alzheimer's disease, would alter neurovascular coupling responses to sensory stimulation.

88 erebrovascular reactivity and whisker-evoked neurovascular coupling responses were measured at end po

89 nt for the full expression of sensory-evoked neurovascular coupling responses.

90 measurements indicate that the mechanism of neurovascular coupling systematically affects the vascul

91 This neurovascular coupling underlies blood oxygen level-depe

92 The mechanisms of neurovascular coupling underlying generation of BOLD fMR

93 s, and reveal a second vascular component of neurovascular coupling upon very strong stimulation.

94 This neurovascular coupling was linked by parvalbumin-express

95 We found that neurovascular coupling was similar across states and tha

96 d hemodynamics, a phenomenon referred to as "neurovascular coupling" (NVC).

97 This relationship is termed 'neurovascular coupling' and it is critical for regulatin

98 Neurovascular coupling, cerebrovascular remodeling and h

99 ked neuronal activity.SIGNIFICANCE STATEMENT Neurovascular coupling, defined as the tight relationshi

100 orts a conceptual shift in the mechanisms of neurovascular coupling, from a unidimensional process in

101 -1 inhibition restores tPA activity, rescues neurovascular coupling, reduces amyloid deposition aroun

102 To quantify changes in neurovascular coupling, we combined laser speckle contra

103 usal state impacts cerebral hemodynamics and neurovascular coupling, we monitored neural activity, be

104 both caveolae and eNOS completely abolished neurovascular coupling, whereas the single mutants exhib

105 aECs, but not in neighbouring SMCs, impaired neurovascular coupling.

106 Isovolumic haemodilution did not alter neurovascular coupling.

107 a longer time span and is less dependent on neurovascular coupling.

108 derstand temporal correlations that describe neurovascular coupling.

109 t release Ca(2+) from stores does not affect neurovascular coupling.

110 y visual cortex to investigate the limits of neurovascular coupling.

111 hese networks, over and above the effects on neurovascular coupling.

112 ishing astrocytes as potential regulators of neurovascular coupling.

113 ulation, endothelial-mediated signaling, and neurovascular coupling.

114 ells (aECs) have an active role in mediating neurovascular coupling.

115 vasoconstriction and a general disruption of neurovascular coupling.

116 ing molecule that plays an important role in neurovascular coupling.

117 ed pathway in aECs is a major contributor to neurovascular coupling.

118 Proper brain function depends on neurovascular coupling: neural activity rapidly increase

119 ated that nitric oxide is a key component of neurovascular coupling; this has yet to be translated to

120 del that incorporates internalization into a neurovascular-coupling relationship.

121 ial stretching, which is ideal in the use in neurovascular curved arteries.

122 he critical role of necroptosis in mediating neurovascular damage and hypoperfusion-induced TAK1 loss

123 Spaceflight-induced potential adverse neurovascular damage and late neurodegeneration are a ch

124 and functional consequences associated with neurovascular damage and late neurodegeneration.

125 In vivo MRI evaluated both the neurovascular damage and the protective effect of exerci

126 nstrate the protective effect of exercise on neurovascular damage in the ageing brain of ApoE(-/-) mi

127 e devastating consequences of stroke-induced neurovascular damage.

128 Concomitant with age-related neurovascular decline and complement activation, astrocy

129 rcise had little to no effect on age-related neurovascular decline or microglia/monocyte activation i

130 Neurovascular decline was sufficient to cause vascular l

131 ed in an excellent outcome without secondary neurovascular deficits in this rare case of traumatic co

132 Neurovascular deficits lead over time to impaired neuron

133 bra was achieved and there were no secondary neurovascular deficits.

134 I/R injury induced neurovascular degeneration, energy failure, DNA damage,

135 lar telangiectasia type 2; MacTel) is a rare neurovascular degenerative retinal disease.

136 ding of the eye, in particular pathological, neurovascular, degenerative processes.

137 poses new questions about the mechanisms of neurovascular development and its role in both normal an

138 ain astrocyte end feet that is essential for neurovascular development and physiology, in the pathoge

139 iggers a strong immune response and disrupts neurovascular development, resulting in postnatal microc

140 gh endothelial WNT signaling is required for neurovascular development, too much endothelial WNT sign

141 ationship between HVS physiology and retinal neurovascular development.

142 microstructure and micron-level features of neurovascular devices, would have a profound impact in t

143 nsion, Imaging, Metabolic & Lipid Disorders, Neurovascular Disease & Dementia, Promoting Health & Pre

144 Despite the importance of neurovascular disease and subsequent injury after ischem

145 ebral cavernous malformation (CCM) is a rare neurovascular disease that is characterized by enlarged

146 nd specific diagnostic microbiome in a human neurovascular disease.

147 dentify caspase-9 as a therapeutic target in neurovascular disease.

148 Acute cerebral ischemia and chronic neurovascular diseases share various common mechanisms w

149 a corresponding growth in those affected by neurovascular diseases, including stroke and dementia.

150 monitoring and therapeutic interventions of neurovascular diseases.

151 sfunction responsible for cardiovascular and neurovascular diseases.

152 Blood-brain barrier (BBB) pathology leads to neurovascular disorders and is an important target for t

153 and stroke are two common and heterogeneous neurovascular disorders responsible for a significant bu

154 ed the greatest tissue specificity; however, neurovascular dyes already enjoy wide clinical use.

155 y unappreciated role of tPA in Abeta-related neurovascular dysfunction and in vascular amyloid deposi

156 le link between astrocytic Apoe, age-related neurovascular dysfunction and microglia/monocyte activat

157 uch as Alzheimer's disease may contribute to neurovascular dysfunction and neurodegeneration associat

158 to BBB breakdown to investigate the role of neurovascular dysfunction in high-fat diet (HFD)-induced

159 investigated whether tPA is involved in the neurovascular dysfunction of Abeta.

160 Although neurovascular dysfunction(3,11) and BBB breakdown develo

161 espite persistent cerebral hypoperfusion and neurovascular dysfunction.

162 hat are associated with pericyte loss and/or neurovascular dysfunction.

163 cause of cerebral cavernous malformation, a neurovascular dysplasia resulting in dilated, thin-walle

164 Neurovascular dysregulation in putaminal and pallidal re

165 re substantiating the beneficial pleiotropic neurovascular effects of chronic statin treatment and pr

166 Amyloid-beta (Abeta) peptides have profound neurovascular effects that may contribute to cognitive i

167 rovascular, memory and epilepsy clinics, and neurovascular emergency services, emphasizing the need f

168 y monocytes with stress adhered to IL-1R1(+) neurovascular endothelial cells and this interaction was

169 NOX1 abundance was also assessed in neurovascular endothelial cells.

170 induced endothelial morphogenesis produced a neurovascular environment.

171 Accordingly, we propose that enlarged neurovascular facial canals shouldn't be used to exclusi

172 prior to the nasal process, a large and deep neurovascular foramen within the perinarial fossa, and a

173 both the neural interactions and a flexible neurovascular forward model.

174 nings of hypertension-induced alterations in neurovascular function during cold exposure is clinicall

175 tension, no studies have examined integrated neurovascular function during cold stress in HTN.

176 tension, no studies have examined integrated neurovascular function during cold stress in hypertensiv

177 ct of STAT3-mediated astrocyte reactivity on neurovascular function in brain metastasis.

178 Studies have shown impaired neurovascular function in several mouse models of AD, in

179 ia is associated with further impairments in neurovascular function.

180 sterolaemia is associated with decrements in neurovascular function; however, little is known about t

181 This position allows them to regulate key neurovascular functions of the brain.

182 l cells, astrocytes and neurons that control neurovascular functions.

183 nockout mice showed diminished expression of neurovascular guidance genes and attenuated retinal vasc

184 A neurovascular guiding factor, Semaphorin 3c (Sema3c), is

185 ifactorial, disabling, recurrent, hereditary neurovascular headache disorder.

186 perience has profound and complex effects on neurovascular health and disease.

187 supports emerging concepts that maintaining neurovascular health promotes brain health.

188 Here, we present a neurovascular high-frequency optical coherence tomograph

189 lecular mechanisms by which VEGF coordinates neurovascular homeostasis has become more sophisticated.

190 According to the neurovascular hypothesis, impairment of low-density lipo

191 promoted anxiogenesis through stimulation of neurovascular IL-1R1 by IL-1beta.

192 themes of modern stroke care are the use of neurovascular imaging and speed of diagnosis and treatme

193 ectronic nicotine delivery system-associated neurovascular impairment is provided, and a model is pro

194 otential for neurogenesis, angiogenesis, and neurovascular inductive activity.

195 ent methods and capture the full spectrum of neurovascular injury and its clinical effect.

196 Neurovascular injury has been proposed as a universal pa

197 development of intracerebral haemorrhage and neurovascular injury in experimental stroke.

198 investigate the role of PGE2 EP1 receptor in neurovascular injury in stroke.

199 ed the effects of these compounds on retinal neurovascular injury induced by hyperglycemia.

200 ion after stroke beyond its acute effects on neurovascular injury.

201 cant alterations in pathways responsible for neurovascular integrity, mitochondrial function, neurona

202 t injury after neonatal stroke by preserving neurovascular integrity, we subjected postnatal day 7 (P

203 We find Mekk3 deficiency impairs neurovascular integrity, which is partially dependent on

204 ha modulates semaphorin 3E transcription and neurovascular interaction in pathological retinal angiog

205 work demonstrates the efficacy of exploiting neurovascular interaction to direct axon growth in the i

206 elial GABA signaling shapes angiogenesis and neurovascular interactions during prenatal development.

207 ental pulp samples revealed 3D-morphological neurovascular interactions that could not be visualized

208 microglia, the blood-brain barrier and other neurovascular interfaces) are important facilitators of

209 ltiradicular teeth were found, also distinct neurovascular interplays.

210 evaluation confirmed osseous, articular, and neurovascular invasion in 8.6%, 2.9%, and 25.3% of patie

211 including extra-compartmental extension and neurovascular invasion.

212 n of MEKK3:CCM2 interaction leads to similar neurovascular leakage.

213 rnous malformations (CCMs) are predominantly neurovascular lesions and are associated with mutations

214 s impaction syndromes, stress fractures, and neurovascular lesions.

215 n the clinically-relevant hour-long state of neurovascular malfunction in the wake of CSDs.

216 htened systemic sNVT and provide a potential neurovascular mechanism for elevated blood pressure in o

217 s is of relevance to neurologists working in neurovascular, memory and epilepsy clinics, and neurovas

218 re evaluated, along with skeletal muscle and neurovascular models.

219 weeks of diabetes, the vasoreactivity of the neurovascular network to CO2 was abolished and was not r

220 r mapping the hemodynamic signal through the neurovascular network with specificity at the level of i

221 ible with lipophilic dyes that highlight the neurovascular network, to obtain high tissue transparenc

222 sion, Imaging, Metabolic Disorders & Lipids, Neurovascular & Neurodegenerative Disorders, Rhythm Diso

223 Furthermore, they reside in a neurovascular niche and have the potential for neurogene

224 By imaging the neurovascular niche in combination with chemogenetic man

225 is of a CD31-enriched cell population of the neurovascular niche showed that endothelial Stat3 ablati

226 g their unique role in maintaining a healthy neurovascular niche, and in supporting brain development

227 ularis, a group of syndromes associated with neurovascular, ophthalmological, overgrowth, and maligna

228 Neurovascular pathologies of the central nervous system

229 delivery nanosystems or contrast agents for neurovascular pathologies.

230 al for developing new interventions to treat neurovascular pathologies.

231 the importance of considering stress-induced neurovascular pathology in depression and provide therap

232 bservations give important information about neurovascular pathophysiology in pediatric CM.

233 In summary, our findings suggest a neurovascular protective effect of GHRH analogs during t

234 s are critical in driving the alterations in neurovascular regulation and attendant cognitive impairm

235 cates that distinct processes might underlie neurovascular regulation for both stimulation and sponta

236 mer disease, induces profound alterations in neurovascular regulation through the innate immunity rec

237 our knowledge of their effects on endogenous neurovascular remodelling events.

238 Nrf2 in reprogramming ischemic tissue toward neurovascular repair via Sema6A regulation, providing a

239 This pronounced alteration of neurovascular response to pressure in patients with DFU

240 as compared to WT mice may explain impaired neurovascular responses in the mutant, and these alterat

241 The new fossil also reveals a neurovascular sensory system in the premaxilla and a par

242 ss central to cerebral malaria pathogenesis: neurovascular sequestration.

243 structural foundation for future studies of neurovascular signaling in health and disease.

244 are confounded by age-related changes in the neurovascular signaling.

245 s review discusses the role of astrocytes in neurovascular signalling in both physiology and patholog

246 Nitric oxide is a vital neurovascular signalling molecule in preclinical models,

247 Hybrid neurovascular spheroids were constructed by fusion of hu

248 nhanced immunoreactivity was observed on the neurovascular structure around hematoma at 24 hrs after

249 ging leads to a significant deterioration of neurovascular structures including basement membrane red

250 may exhibit tumor growth involving critical neurovascular structures or diffuse growth, resulting in

251 structures (muscles, tendons, ligaments, and neurovascular structures) and of associated lesions.

252 eth, a platyrostral rostrum with a developed neurovascular system, an elongate neck, bizarrely-propor

253 ort for functional dopamine transport at the neurovascular terminals, shedding light on a long-standi

254 trial and other studies have shown that the neurovascular thrombectomy improves outcomes at 90 days

255 INTERPRETATION: At 12 months follow-up, neurovascular thrombectomy reduced post-stroke disabilit

256 ing intravenous alteplase when eligible) and neurovascular thrombectomy with Solitaire FR or medical

257 e present study, we aimed at constructing 3D neurovascular tissues by combining in vitro neurogenesis

258 ture models and succeeded in constructing 3D neurovascular tissues with an optimized seeding conditio

259 thetic vasomotor outflow, termed sympathetic neurovascular transduction (sNVT), accompanied changes i

260 It is unknown whether IH alters sympathetic neurovascular transduction (sNVT), measured as the relat

261 es in resting-state connectivity, to explore neurovascular uncoupling as a mechanism underlying these

262 Neurovascular uncoupling by cocaine during stimulation b

263 Neurovascular uncoupling could contribute to cocaine's n

264 ty may be false-negative results driven by a neurovascular uncoupling mechanism.

265 n of PAI-1 increased tPA activity, prevented neurovascular uncoupling, and ameliorated cognition in 1

266 responses to neuronal stimuli, resulting in neurovascular uncoupling, reduced oxygen supply to the b

267 Neurovascular unit (NVU) is a basic unit in the brain, i

268 ithin the greater context of a multicellular neurovascular unit (NVU) that includes neurons, astrocyt

269 Age-related changes to the neurovascular unit (NVU), and their consequences for cer

270 The concept of the neurovascular unit (NVU), formalized at the 2001 Stroke

271 TEMENT: Pericytes are a key component of the neurovascular unit and are essential for normal BBB func

272 Given the role of APOE in maintaining the neurovascular unit and as an anti-inflammatory molecule,

273 affects the brain through compromise of the neurovascular unit and astrocyte injury.

274 s support bidirectional signaling within the neurovascular unit and astrocytes as key modulators of P

275 ighly interactive processes that involve the neurovascular unit and neural stem cells.

276 should be able to target the multi-cellular neurovascular unit and the therapeutic relationships amo

277 They are positioned centrally in the neurovascular unit between endothelial cells, astrocytes

278 CNS pericytes are uniquely positioned in the neurovascular unit between endothelial cells, astrocytes

279 issue of the JCI points to perturbations of neurovascular unit coupling caused by perivascular macro

280 Intravenously injected DAG peptide homes to neurovascular unit endothelial cells and to reactive ast

281 the blood-brain barrier (BBB), a specialized neurovascular unit evolved to maintain brain homeostasis

282 ese cells to the structural integrity of the neurovascular unit has not hitherto been assessed.

283 increasing appreciation for the role of the neurovascular unit in neurodegenerative diseases.

284 lutes through the paracellular spaces in the neurovascular unit is a key mechanism in CNS calcificati

285 multi-targeting capabilities, using in vitro neurovascular unit models and an in vivo model of AD.

286 Here, we employed a multicellular 3D neurovascular unit organoid containing human brain micro

287 astrocytes, and microglia, cell types in the neurovascular unit that can secrete MMPs.

288 contribution to cellular interactions at the neurovascular unit that influence the overall function o

289 human iPSC-derived tissue, we have created a neurovascular unit that recapitulates complex BBB functi

290 Astrocytes are an integral component of the neurovascular unit where they act as homeostatic regulat

291 volved in the ischaemic death process at the neurovascular unit, an improved preselection and evaluat

292 mmunication between the affected brain area, neurovascular unit, and peripheral immune cells.

293 At the neurovascular unit, brain endothelial cells, astrocytes,

294 ay, we searched for molecular markers of the neurovascular unit, including endothelial cells and astr

295 The neurovascular unit, which includes neurons, glial cells,

296 multiple cellular involvement affecting the neurovascular unit.

297 d endothelial cells, which together form the neurovascular unit.

298 etween neurons, vasculature, and glia within neurovascular units are critical for maintenance of the

299 ons, the amacrine and horizontal cells, form neurovascular units with capillaries in 2 of the 3 retin

300 However, the heterotypic interactions of neurovascular units, composed of neurons, pericytes, ast